The intravenous injection of F1 hybrid mice with parental T cells result in a loss in the ability of the F1 mice to generate T-cell mediated immune response in vitro to graft-versus-host immune deficiency (GVHID). Recognition of host class II MHC antigens by donor cells in required to initiate GVHID. Recognition of host class I MHC antigens may or may not induce GVHID, depending on the class I determinants required. Recognition of class II only abrogates L3T4+T helper cell responses but not Lyt2+ T helper cell responses; recognition of class I and II results in loss of both L3T4+ and Lyt2+ T helper cell responses. Induction of GVHID by class I and II recognition requires both L3T4+ and Lyt2+ cells; induction of GVHID by class II only recognition requires only L3T4+ parental T cells. Inoculation of parental T cells into F1 mice can also result in different immune abnormalities, depending on the donor and host strains used. Injection of C57BL/6 cells into B6D2F1 mice resulted in extensive immune suppression, hypogammaglobulinema, and susceptibility to infection. Injection of DBA/2 into B6D2F1 mice result in selective suppression of L3T4+ T helper cell function, hypergammaglobulinema, and autoantibody production with SLE-like symptoms. The differences in these two forms of SLE were attributed to a defect in DBA/2 anti-F1 CTL precursor frequency. The patent-into-F1 GVH reaction also results in severe defects in bone marrow stem cell function, as well as in a defect in the self MHC restriction ability of the F1 thymus.